By Henry G. Kunkel, Frank J. Dixon (Eds.)
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Extra resources for Advances in Immunology, Vol. 33
These findings demonstrate that F, male B cells have a defect in their ability to respond to the T D antigen SRBC in the presence of T cells which provide sufficient help to F, female B cells. The capacity of the F, male B cells to respond to SRBC was considerably improved if the B cells were derived from mice that had been primed to SRBC. Different results were obtained by E. Metcalf et al. (1980) who demonstrated that the IgM and IgG anti-TNP responses of these mice to TNP-KLH were equivalent to normals.
It also was noted in this study that the frequency of B cells responding to B-cell mitogens present in FCS was “at least 10-fold” less in immune defectives than in normals. The LPS or poly(1-C)-induced proliferative responses of B cells derived from young adult vs aged immune-defective mice have been studied. , in preparation) (see Sections III,A,2, III,A,4, and VI,6). , 1980; Nariuchi and Kakiuchi, 1981),and human B cell-activating factors (Cameron and Wood, 1978)has also been studied. PPD functioned like LPS and poly(1-C) in that it induced lower proliferative responses in B cells from immune-defective as compared to normal mice.
However, when lethally irradiated F, mice were reconstituted with primed F1 T cells, along with B cells (anti-Thy treated spleen or bone marrow) from F, male mice, they made approximately 10-fold lower IgM or IgG antiSRBC responses than mice reconstituted with F, female B cells (Fig. , 1979). Increasing the number of F, male B cells or primed T cells in these adoptive transfer experiments did not alter the low responses. These findings demonstrate that F, male B cells have a defect in their ability to respond to the T D antigen SRBC in the presence of T cells which provide sufficient help to F, female B cells.
Advances in Immunology, Vol. 33 by Henry G. Kunkel, Frank J. Dixon (Eds.)